Further observations on calcium and other divalent cations metabolism in intact Ehrlich ascites tumour cells.
The metabolism of calcium has been investigated in the Ehrlich Ascites Tumour Cells (ATC). ATC extrude Ca2+ actively by an energy-dependent mechanism, supported by both respiration and glycolysis. Extrusion takes place even against a very steep concentration gradient (10 mM Ca2+). Cell calcium content is decreased by monovalent cations (Na+,K+ and Li+), which act independently from their metabolic effects. La3+ inhibits ATC Ca2+ extrusion whereas Ruthenium Red slightly decreases cell calcium content. The antibiotic ionophore A 23187 strongly increases ATC Ca2+ level. the metabolism of other divalent cations (Mg2+, Sr2+ and Mn2+) has been studied. Mg2+ does not show appreciable changes in the various metabolic conditions tested, while Mn2+ and Sr2+ behave quite differently from Ca2+, suggesting a different distribution of these cations in ATC. The experimental findings indicate that Ehrlich Ascites Tumour Cells regulate their calcium content by mechanisms related to plasma membranes while the size and activity of mitochondrial compartment is of minor importance.
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism*; D002413:Cations, Divalent; D002462:Cell Membrane / Q000187:drug effects; D007811:Lanthanum / Q000494:pharmacology; D008274:Magnesium / Q000378:metabolism; D008345:Manganese / Q000378:metabolism; D051379:Mice; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology; D013324:Strontium / Q000378:metabolism
D002413:Cations, Divalent; C028521:lanthanum chloride; D000001:Calcimycin; D008345:Manganese; D007811:Lanthanum; D012964:Sodium; D008274:Magnesium; D011188:Potassium; D002118:Calcium; D013324:Strontium